Sleep is a mental and physical state in which one becomes inactive and unconscious of the environment around him or her (Borbély, 2003). In the real sense sleep is just a partial disconnection from the world in which outside stimuli are obstructed from the senses. Normal sleep is indentified by a general reduction in most of the body functions including blood pressure, temperature, and the breathing rate. This is contrast to the human brain that never reduces in activity.
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The brain is always active whenever a person is a wake or a sleep (Berger, 2007). A normal human being sleeps for eight hours. These eight hours are divided into two equal parts. The first part is the rapid eye movement, and the second is the non-rapid eye movement. The two parts form a cycle (Ishimori, 2004). The intention of this paper is to look at the basis of sleep in relation to the biological mechanisms that cause people to sleep and stay awake.
History of Sleep
The history of sleep is believed to have been introduced by a psychologist professor at the University of Nagoya in Japan about one hundred years ago (Bayliss, 2006). The psychologist proposed a theory that explains the concept of sleep regulation.
Kuniomi Ishimori and Heni Pieron neuroscientist state that, a hormonal chemical and not the neural network (Ishimori, 2004) cause sleep regulation. In earlier researches, researchers took some samples that were sterilized and dialyzed from dogs that had sleep then injected to the brains of the dogs that had no sleep. The dogs that received these samples fell after a short time.
The scientists went ahead and took samples from normal dogs that did not have any sleep then introduced into the brains of other normal dogs without any sleep (Berger, 2007). The response showed that the recipient dogs did not sleep. This research indicated that there are substances that cause sleep known as “endogenous sleep-promoting substances.” Although the contradiction fact is that the nature of the chemical substances that caused sleep was not identified.
Various research groups carried out their research and reported more than thirty endogenous sleep causing substances. In most cases, their physiological relevance was uncertain. Tokyo igakkai Zasshi from Japan published the first Ishimori’s paper entitled “true cause of sleep _ a hypogenic substance as evidenced in the brain of sleep deprived animals,” in the year 1909.
Ishimori made further suggestion that when a person continuously stays a wake, it may also cause accumulation of factors that cause sleep in the brain (Borbély, 2003). Currently this is referred to as homeostatic sleep regulation. Starling and Bayliss discovered “scretin” in 1902. This is in relation with the existence of blood-borne messengers. The new idea of hormonal control of the body functioning became quite fashionable and popular in those days.
Hans Berger a Germany neurologist in Jena invented an electroencephalogram (EEG) that records brain waves in 1920s. The discovery facilitated the qualitative and quantitative analysis of sleep. Until then, sleep was regarded as an unapproachable phenomenon mainly because it could not be explained scientifically.
Kleitman and his coworkers discovered rapid eye movement (REM) sleep in Chicago. This discovery took place in the year 1953 in human beings (Bayliss, 2006). Jouvet and his group in Lyon identified that sleep is never a uniform phenomenon, and it consists of two main different stages.
Sleep and wakefulness are the major complex, phenomena. Furthermore, sleep is divided into two parts: the REM and the non-REM sleep can easily be determined by examining the animal’s behavior (Berger, 2007). The authors suggest that it needs more accurate measurement of sleep and wake pattern by the use of the electrooculogram (EOG), the recording of the movement of the eye, EEG and (EMG) electromyogram, the recording of the tension of the muscles (Ishimori, 2004).
When a normal, healthy person goes to sleep at eleven, the first step in sleeping starts with the NREM and then followed by the REM sleep. This makes a cycle in the sleeping pattern. As in the example, it all begins with the NREM that which progressively becomes deeper.
It takes around four to five cycles in which one take about 90 minutes; arousal comes after the concluding REM sleep (Borbély, 2003). This principle has been in existence for a long time and yet the physiological regulatory mechanisms and the meaning have completely remained a mystery.
Alexander Borbely from the Zurich University in Switzerland came up with his two famous process model that show sleep regulation in 1982. He argues that homeostatic process is entirely controlled by sleep pressure or sleep propensity that build up during the wakefulness period. The process is related to the Ishimori’s thus the name Ishimori-Pieron type.
On the other hand, a biological or pacemaker clock that is independent of the prior waking and sleep determines the circadian process well known as the sleep-wake sequence during the night and day. This clock is found in the body of the animals. Researches indicate that Ultradian process can generate alternation of REM and NREM sleep (Piéon, 2003). From a scientific point of view, the molecular mechanisms that explain the sleep- wake regulation in all the processes have remained unknown.
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Sleep and Prostaglandin
Prostaglandins (PGs) are the lipid mediators (Bayliss, 2006). There are more than thirty kinds of prostanoids, which are known worldwide. The compounds are distributed extensively in all mammalian organs and tissues.
They have a diverse and numerous biological effects on various pathological and physiological activities in the body, and that is why they are sometimes called local or tissue hormones. In 1980s, the scientists discovered the most common prostanoid in the mammalians and mostly the rats and human beings (Berger, 2007).
According to their findings, they suggest that PGD2 can be a distinctive component of the brain and might be having some essential function in the organ. They found out that when PGD2 cause sleep to rats when it is microinjected in the brains (Piéon, 2003). This was a notable achievement, and they decided to carry on with the study to the molecular mechanism and the physiological significance.
Inoue and Honda from Tokyo Japan first designed the bioassay analysis system for sleep. The analysis of the structure is as follows: through microinjection pump, the chemical PGD2 is injected gradually and constantly through a cannula which is chronically rooted in the 3rd ventricle of a rat . The stages that the rat undergoes to sleep are determined using polygraphic recording of EMG and EEG.
Other aspects like food intake, water intake and brain temperature, are monitored and the general behavior of the rat is recorded using a video recorder under infra-red light. The rats are nocturnal animals that sleep most of the daytime, and remain active during the night. The outcome of the research showed that when the PGD was constantly injected in the third ventricle of a rat, the REM and the NREM sleep improved significantly during injection time.
PGD2 caused the effect since the other PGs were ineffective (Borbély, 2003). The experiment mostly depended on the dose and the little picomolar quantity of PGD2 given to per minute it was enough to cause excess sleep to the rat. The quantity of the PGD2 that required causing sleep corresponded quite closely to the normal concentration inside the brain (Piéon, 2003).
The results indicated that pharmacologically high doses are not necessary, and it can imply that the difference in the concentrations of PGDs which ordinarily occur in the brain have the ability to control sleep under physiological circumstances (Berger, 2007).
The most important aspect is that the PGD2 stimulated sleep was the same as the physiological sleep just as shown by electrophysiological principle and conduct that involves power spectral data. Contrary to PGE2, the PGD2 is never pyrogenic, but in the real sense, it caused little amounts of reduction in temperature as seen to happen throughout the physiological sleep (Ishimori, 2004).
Others experiments, that were carried out, in Japan with monkeys, Mocaca mulatta, indicated clearly that PGD2 could induce natural or physiological sleep (Bayliss, 2006). The sleeping pills and drugs cause quite different sleep from the physiological sleep or the natural one. This shows that PGD2 is a true sleep hormone.
The discoveries in the experiments above explain how sleep can be introduced to an animal from the beginning until it gets into a deep sleep. Then the next part is to identify if the same experiment can apply in the process of waking up the animal from the sleep explaining the wake sleep process.
Philos published the brief summary of the experiment in the year 2000. The article observes that the main enzyme that induces sleep is mainly found in the arachnoid membrane and the choroid plexus.
After this enzyme is generated, PGD2 is secreted into cerebrospinal fluid (CSF) and then flows inside the subarachnoid and ventricular spaces. The PDG receptors known as the DPRs are localized on the little area on the ventro-rostral plan of the basal forebrain. PGD2 that circulates in the CFS binds the receptors at the point where the sleep signal is generated (Piéon, 2003).
The signal passes through the parenchyma brain to the ventrolateral preoptic area VLPO), which is a centre for sleep, across the pia membrane (Ishimori, 2004). The process is mediated through adenosine by A2A adenosine receptor. VPLO cast to the tuberomammilary centre (TMN) (Berger, 2007).
The scientists, Oishi and coworkers, found out that adenosine from the TMN cause sleep by hindering the histamnergic structure via A1 receptor (Bayliss, 2006). This implies that PGD2 induce sleep by facilitating the functioning of sleep neurons (Borbély, 2003).
On the same point, wake materials like orexin or PGE2 thruogh the histamine mechanism support an organisms’ wakefulness. According to the scientists, it is their view that the work on wakefulness still requires great attention and it forms the basis of greater basis for more investigation.
Stages of sleep
Sleep has four main stages. It starts from dozing and continuously progresses into a unusually deep sleep.
The stage is can be termed as a doing stage. In this stage, five percent of the non-REM is spent. It is the transitional phase of the exact light sleep. The birthing rate, and the muscles start to relax and a person can be easily awakened (Berger, 2007). A person may feel a hypnic jerk during this period, the tendency to fall asleep and come back easily. After the rush of activities, the body starts to get into a slight slumber. The EEG at this stage is low, and the eye movements are slow. The eyes roll slowly as though closing and opening.
This is the official onset of a consolidated sleep. A bout forty-five percent of the non-REM sleep is covered in this step (Piéon, 2003). The eye movement stops then the brain waves enlarge. There are two distinct brain waves in this stage, K-complexes and spindles (Borbély, 2003).
A sleep spindle is a design by which EEG waves that consist of a burst of eleven to fifteen hertz wave that last from five to fifteen seconds. A K complex has quite a high voltage of EEG activity. It consists of a sharp downward constituent then followed by a slow upward constituent. This pattern lasts for over five seconds.
As the sleep advances deeper and deeper, it becomes extremely difficult to arouse someone at this stage. An individual may spend about twelve percent of the non-REM sleep in stage three. Real slow wave sleep starts with slow and large wave in amalgamate little, faster ones.
This stage is normally characterized by extremely deep sleep. It mostly spends round seventy-five percent non-REM sleep, and thirteen percent of this part is spent in the last stage (Berger, 2007). An individual in the last two stages is more difficult to wake than an individual who is in the first two stages (Bayliss, 2006). People who wake up from sleep normally feel disoriented and groggy for some time.
This is the period that a person may experience dreams. During this time, there is an irregular breathing, periodic eye flattering, there is also an irregular heart rate, blood pressure and body temperature. This makes a difference between non-REM and REM sleep stages (Ishimori, 2004).
In other words, the REM is referred to as paradoxical sleep since brain wave activities is almost similar to a wakened state. During this stage, the brain obstructs all signals towards the muscles and they remain immobile so that the dreams cannot be acted out (Piéon, 2003). Most adults spend a round twenty to twenty-five percent of their sleep in REM.
The biological basis of sleep is dated back to more than one hundred years ago. Kuniomi Ishimori and Heni Pieron laid the foundation of sleep through their research done in Japan. The later physiologists identified that sleep can be classified into two main groups. These are the REM and the non-REM (Bayliss, 2006).
All the two parts come in different stages, that is beginning from stage one up to stage four, all the stages follow one another from the beginning of sleep to the time a person wakes up. There is still more room for other scientists to make the research and prove the sleep phenomenon.
- Top of page
- HISTORICAL INTRODUCTION
- PROSTAGLANDIN (PG) AND SLEEP
- PROSTAGLANDIN (PG) D SYNTHASE, THE KEY ENZYME IN SLEEP REGULATION
- MOLECULAR MECHANISMS OF SLEEP–WAKE REGULATION BY PGD2 AND E2
- ROLE OF PGD2 IN THE CIRCADIAN PROCESS
- THE ROLE OF PGD2 IN THE HOMEOSTATIC PROCESS
- HUMAN EXPERIMENTS
- IN SUMMARY
- CONFLICT OF INTERESTS
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Berger, H. (2007). Über das Elektrenkephalogramm des Menschen. J. Psychol. Neurol. Chicago: Harvard Publishers
Borbély, A.A. (2003). Two process model of sleep regulation. Hum. Neurobiol. New York: Macmillan Publishers
Ishimori, K. (2004). True cause of sleep – a hypnogenic substance as evidenced in the brain of sleep-deprived animals. Tokyo: Igakkai Zasshi.
Piéon, H. (2003). Le probléme physiologique du sommeil. Paris: Masson et cie.